Prospective evaluation of gastric acid secretion and cobalamin absorption following gastric bypass for clinically severe obesity

K. E. Behrns, C. D. Smith, M. G. Sarr

Research output: Contribution to journalArticle

107 Citations (Scopus)

Abstract

The pathophysiologic mechanism(s) responsible for cobalamin deficiency after Roux-en-Y gastric bypass for clinically severe obesity remains unexplained. Inadequate secretion of intrinsic factor has been postulated, but decreased gastric acid secretion resulting in maldigestion and inadequate liberation of free cobalamin from its native protein-bound form is also possible. The aim of this study was to determine prospectively secretion of gastric acid and absorption of crystalline (free) and protein-bound cobalamin before and after gastric bypass. Eight patients (two men, six women) underwent orogastric intubation of the intact stomach preoperatively and the proximal gastric pouch postoperatively. Gastric acid secretion in the basal and stimulated (pentagastrin, 6 μg/kg) states was determined by a perfused, nonabsorbable marker technique to quantitate recovery of gastric secretion. Absorption of radiolabeled (57Co) crystalline and protein-bound cobalamin was assessed on separate days by 24-hr urinary excretion. After gastric bypass, acid secretion (x̄ ± SEM) was markedly reduced in basal (9.1 ± 3.6 vs 0.005 ± 0.003 meq/hr; P = 0.04) and stimulated (12.8 ± 1.8 vs 0.008 ± 0.003 meq/30 min; P = 0.002) states. Absorption of crystalline cobalamin was decreased (15.8 ± 2.5 vs 9.4 ± 1.4%; P = 0.08) to a lesser extent than was protein-bound cobalamin (5.9 ± 1.0 vs 1.1 ± 0.3%; P = 0.004). In summary, gastric acid secretion from the gastric pouch is negligible after gastric bypass, and food-bound cobalamin is maldigested and subsequently malabsorbed presumably due to pouch achlorhydria. Decreased absorption of free cobalamin suggests decreased cobalamin-intrinsic factor complex formation. This study suggests that cobalamin deficiency after Roux-en-Y gastric bypass results both from inadequate digestion of food-bound cobalamin and from insufficient secretion of intrinsic factor.

Original languageEnglish (US)
Pages (from-to)315-320
Number of pages6
JournalDigestive Diseases and Sciences
Volume39
Issue number2
StatePublished - 1994

Fingerprint

Gastric Bypass
Morbid Obesity
Gastric Acid
Vitamin B 12
Intrinsic Factor
Stomach
Proteins
Achlorhydria
Food
Pentagastrin
Intubation
Digestion

Keywords

  • absorption
  • bariatric surgery
  • clinically severe obesity
  • cobalamin
  • gastric acid secretion
  • intrinsic factor
  • morbid obesity
  • obesity

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Prospective evaluation of gastric acid secretion and cobalamin absorption following gastric bypass for clinically severe obesity. / Behrns, K. E.; Smith, C. D.; Sarr, M. G.

In: Digestive Diseases and Sciences, Vol. 39, No. 2, 1994, p. 315-320.

Research output: Contribution to journalArticle

@article{89e6c7219057422293736936090cb299,
title = "Prospective evaluation of gastric acid secretion and cobalamin absorption following gastric bypass for clinically severe obesity",
abstract = "The pathophysiologic mechanism(s) responsible for cobalamin deficiency after Roux-en-Y gastric bypass for clinically severe obesity remains unexplained. Inadequate secretion of intrinsic factor has been postulated, but decreased gastric acid secretion resulting in maldigestion and inadequate liberation of free cobalamin from its native protein-bound form is also possible. The aim of this study was to determine prospectively secretion of gastric acid and absorption of crystalline (free) and protein-bound cobalamin before and after gastric bypass. Eight patients (two men, six women) underwent orogastric intubation of the intact stomach preoperatively and the proximal gastric pouch postoperatively. Gastric acid secretion in the basal and stimulated (pentagastrin, 6 μg/kg) states was determined by a perfused, nonabsorbable marker technique to quantitate recovery of gastric secretion. Absorption of radiolabeled (57Co) crystalline and protein-bound cobalamin was assessed on separate days by 24-hr urinary excretion. After gastric bypass, acid secretion (x̄ ± SEM) was markedly reduced in basal (9.1 ± 3.6 vs 0.005 ± 0.003 meq/hr; P = 0.04) and stimulated (12.8 ± 1.8 vs 0.008 ± 0.003 meq/30 min; P = 0.002) states. Absorption of crystalline cobalamin was decreased (15.8 ± 2.5 vs 9.4 ± 1.4{\%}; P = 0.08) to a lesser extent than was protein-bound cobalamin (5.9 ± 1.0 vs 1.1 ± 0.3{\%}; P = 0.004). In summary, gastric acid secretion from the gastric pouch is negligible after gastric bypass, and food-bound cobalamin is maldigested and subsequently malabsorbed presumably due to pouch achlorhydria. Decreased absorption of free cobalamin suggests decreased cobalamin-intrinsic factor complex formation. This study suggests that cobalamin deficiency after Roux-en-Y gastric bypass results both from inadequate digestion of food-bound cobalamin and from insufficient secretion of intrinsic factor.",
keywords = "absorption, bariatric surgery, clinically severe obesity, cobalamin, gastric acid secretion, intrinsic factor, morbid obesity, obesity",
author = "Behrns, {K. E.} and Smith, {C. D.} and Sarr, {M. G.}",
year = "1994",
language = "English (US)",
volume = "39",
pages = "315--320",
journal = "Digestive Diseases and Sciences",
issn = "0163-2116",
publisher = "Springer New York",
number = "2",

}

TY - JOUR

T1 - Prospective evaluation of gastric acid secretion and cobalamin absorption following gastric bypass for clinically severe obesity

AU - Behrns, K. E.

AU - Smith, C. D.

AU - Sarr, M. G.

PY - 1994

Y1 - 1994

N2 - The pathophysiologic mechanism(s) responsible for cobalamin deficiency after Roux-en-Y gastric bypass for clinically severe obesity remains unexplained. Inadequate secretion of intrinsic factor has been postulated, but decreased gastric acid secretion resulting in maldigestion and inadequate liberation of free cobalamin from its native protein-bound form is also possible. The aim of this study was to determine prospectively secretion of gastric acid and absorption of crystalline (free) and protein-bound cobalamin before and after gastric bypass. Eight patients (two men, six women) underwent orogastric intubation of the intact stomach preoperatively and the proximal gastric pouch postoperatively. Gastric acid secretion in the basal and stimulated (pentagastrin, 6 μg/kg) states was determined by a perfused, nonabsorbable marker technique to quantitate recovery of gastric secretion. Absorption of radiolabeled (57Co) crystalline and protein-bound cobalamin was assessed on separate days by 24-hr urinary excretion. After gastric bypass, acid secretion (x̄ ± SEM) was markedly reduced in basal (9.1 ± 3.6 vs 0.005 ± 0.003 meq/hr; P = 0.04) and stimulated (12.8 ± 1.8 vs 0.008 ± 0.003 meq/30 min; P = 0.002) states. Absorption of crystalline cobalamin was decreased (15.8 ± 2.5 vs 9.4 ± 1.4%; P = 0.08) to a lesser extent than was protein-bound cobalamin (5.9 ± 1.0 vs 1.1 ± 0.3%; P = 0.004). In summary, gastric acid secretion from the gastric pouch is negligible after gastric bypass, and food-bound cobalamin is maldigested and subsequently malabsorbed presumably due to pouch achlorhydria. Decreased absorption of free cobalamin suggests decreased cobalamin-intrinsic factor complex formation. This study suggests that cobalamin deficiency after Roux-en-Y gastric bypass results both from inadequate digestion of food-bound cobalamin and from insufficient secretion of intrinsic factor.

AB - The pathophysiologic mechanism(s) responsible for cobalamin deficiency after Roux-en-Y gastric bypass for clinically severe obesity remains unexplained. Inadequate secretion of intrinsic factor has been postulated, but decreased gastric acid secretion resulting in maldigestion and inadequate liberation of free cobalamin from its native protein-bound form is also possible. The aim of this study was to determine prospectively secretion of gastric acid and absorption of crystalline (free) and protein-bound cobalamin before and after gastric bypass. Eight patients (two men, six women) underwent orogastric intubation of the intact stomach preoperatively and the proximal gastric pouch postoperatively. Gastric acid secretion in the basal and stimulated (pentagastrin, 6 μg/kg) states was determined by a perfused, nonabsorbable marker technique to quantitate recovery of gastric secretion. Absorption of radiolabeled (57Co) crystalline and protein-bound cobalamin was assessed on separate days by 24-hr urinary excretion. After gastric bypass, acid secretion (x̄ ± SEM) was markedly reduced in basal (9.1 ± 3.6 vs 0.005 ± 0.003 meq/hr; P = 0.04) and stimulated (12.8 ± 1.8 vs 0.008 ± 0.003 meq/30 min; P = 0.002) states. Absorption of crystalline cobalamin was decreased (15.8 ± 2.5 vs 9.4 ± 1.4%; P = 0.08) to a lesser extent than was protein-bound cobalamin (5.9 ± 1.0 vs 1.1 ± 0.3%; P = 0.004). In summary, gastric acid secretion from the gastric pouch is negligible after gastric bypass, and food-bound cobalamin is maldigested and subsequently malabsorbed presumably due to pouch achlorhydria. Decreased absorption of free cobalamin suggests decreased cobalamin-intrinsic factor complex formation. This study suggests that cobalamin deficiency after Roux-en-Y gastric bypass results both from inadequate digestion of food-bound cobalamin and from insufficient secretion of intrinsic factor.

KW - absorption

KW - bariatric surgery

KW - clinically severe obesity

KW - cobalamin

KW - gastric acid secretion

KW - intrinsic factor

KW - morbid obesity

KW - obesity

UR - http://www.scopus.com/inward/record.url?scp=0028215061&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028215061&partnerID=8YFLogxK

M3 - Article

C2 - 8313814

AN - SCOPUS:0028215061

VL - 39

SP - 315

EP - 320

JO - Digestive Diseases and Sciences

JF - Digestive Diseases and Sciences

SN - 0163-2116

IS - 2

ER -